Diabetes Flashcards
What are two physiological causes of diabetes
- Decreased insulin secretion/insulin deficiency
- decreased insulin sensitivity/insulin resistance
Could be caused by either or both.
Chronic hyperglycemia leads to
Organ and nerve damage throughout the body
Insulin is
a hormone produced by beta islet cells in the pancreas, which helps bring glucose from blood to muscle, and excess is stored in the liver (glycogen) and fat cells (FFA) for energy reserve
What is glycogen
Produced in the muscle and liver through glycogenesis to help store glucose (signaled by insulin)
What is glucagon, how does it work
A hormone that works the opposite way as insulin and is produced by alpha cells in the pancreas. Released when BG is low, it helps the liver to start glycogenolysis and release glucose into the blood stream. In fat tissue it signals FFA’s to make ketones
What happens when glycogen is depleted
Glucagon is released and acts on fat tissue to cause FFA’s to make ketones, and ketones are used as energy
What is type 1 diabetes
~5% of cases- mostly dx in children
- autoimmune destruction of beta islet cells and insulin can’t be produced
- Family history is the largest risk factor
- must tx with insulin
-screen for other autoimmune disorders like celiac and thyroid issues
Patients commonly present with DKA and then are diagnosed
What is diabetic ketoacidosis (DKA)
When the body is not storing glucose from the blood into cells, so the BG is so high, and the cells are so hungry, that the glucagon is released to fat tissue to metabolize FFA into ketones at high amounts.
This is often the initial presentation for T1DM
How do we test and see if a person has T1DM
C- peptide test
- it is released by the pancreas only when the pancreas actually releases insulin
- if very low levels, we dx T1DM
What is T2DM
- Caused by both insulin resistance and insulin deficiency
- Beta islet cells become damaged over time and make less insulin
- onset of disease often unnoticed because hyperglycemia develops gradually; older patients are dx
- assoc. with obesity, FH, physical inactivity, and other comorbidities
- tx with lifestyle modifications in few, most +/- medications
What is prediabetes and how do we treat?
A1c% = 5.7-6.4
FBG = 100-125
2hrPP = 140-199
Prevention of progression: diet and exercise, monitor DM progression annually and treat CVD risk factors
Could treat with metformin to improve BG levels esp. if they have these risk factors: BMI is > 35 , they are < 60 yrs, or they had a hx of gestational DM
What happens to mothers and babies
when gestational diabetes occurs
- Mother is tested between 24-28 weeks using OGTT, hyperglycemia should be treated with lifestyle modifications and medication if needed ( insulin preferred then metformin or glyburide)
-babies are larger than normal (macrosomia) and at higher risk for obesity and diabetes later - the mother is more likely to develop T2DM later and the babies BG is likely to go too low right after birth bc no longer depending on mothers BG
- Mother’s BG goals are very strict (no A1c goal, but fasting </= 95, 1hr PPG </=140, 2hrPPG </=120)
What are patient criteria where we could start metformin
- prediabetes (A1c% 5.7-6.4 or FBG: 100-125, or 2HRPP: 120-189
-BMI >/= 35 kg/m^2 - younger than 60
- history of gestational DM (GDM)
we should monitor annually for the development of diabetes and treat modifiable risk factors
Risk factors for prediabetes and T2DM diabetes
- lack of physical activity*
- overweight (BMI > 25 kg/m2 or 23 in Asian Americans)*
- central obesity (fat in tummy)
- high risk race or ethnicity: anyone who’s not white*
- history of gestational diabetes*
- A1C > 5.7%*
- first degree relative with diabetes*
- HDL < 35 mg/dL or TG > 250 mg/dL
- HTN (>/=140/90 mmHg) or taking BP meds
- CVD history
- Smoking history
- Condition that causes insulin resistance (acanthosis nigricans, PCOS)
Symptoms of hyperglycemia
- the P’s: excessive urination (polyuria), thirst (polydipisia), and hunger (polyphagia)
- fatigue
- blurry vision
- erectile dysfunction (due to vessel destruction) (note: when someone has ED we may check if they also have DM or Cardiovascular issues)
- vaginal fungal infections
Screening for diabetes
- risk for T2DM increases with age, so test everyone starting at age 35
- test all asymptomatic children, adolescents, and adults who are overweight > 25 BMI or 23 in asian Americans and have at least one other risk factor for diabetes; if normal retest q3yrs
How is T2DM diagnosed
- Lab sent Hemoglobin A1c test (>6.5%) tells the average BG in past 3 months or
- Fasting plasma glucose (FPG) (>/= 126 mg/dL) at least 8 hrs post meal or
- OGTT (>/= 200 mg/dL) 2 hrs after drinking glucose liquid
None are preferred more than another, but for FPG and A1C we must get two abnormal results from the same or different tests to confirm diagnosis UNLESS we also have a clear clinical dx. (e.g. classic symptoms of hyperglycemia + BG >/= 200)
Point of care A1c tests are NOT recommended for diagnosing.
Treatment goals for DM (non pregnant)
Non pregnant:
A1c : < 7 or 6.5 if possible without significant hypoglycemia or <8 if the person has low life expectancy or gets severe hypoglycemia; test q3months if not at goal and q6 months if at goal
Preprandial BG: 80 - 130 mg/dL
2 hr PPG: < 180 mg/dL
Treatment goals for Gestational DM
- Mother’s BG goals are very strict (no A1c goal, but fasting </= 95, 1hr PPG </=140, 2hrPPG </=120)
What is the relationship between A1c and eAg
A1c of 6% = eAg of 126 mg/dL, for every increase in A1c by 1%, there is a 28 mg/dL increase in estimated average glucose
ex: A1c of 7% means the eAg is 126 + 28 = 154 mg/dL
What lifestyle modifications can we education patients on to lower BG, improve cholesterol, and BP?
- Goal waist circumference of <35 inches in females, <40 inches in males
- Overweight or obese pts should lose > 5% of their body weight and medications or surgery can help
- Consume natural carbs, avoid or limit alcohol (can hinder insulins act and lead to DKA)
- T1DM patients should use carbohydrate counting with mealtime (prandial) doses (15 g carbs = 1 slice of bread, 1/3 cup of rice/pasta, or 1 piece of fruit)
- at least 150 minutes of moderate exercise/week and reduce sedentary lifestyle by standing every 30 min at least.
- quit smoking
What long term complications can we prevent with glycemic control?
Macrovascular diseases (same as atherosclerotic cardiovascular disease - ASCVD) : large vessels
- CAD (ex: MI, atherosclerosis, different heart diseases)
- Cerebrovascular disease (ex: stroke)
- Peripheral artery disease (PAD) - like atherosclerosis in vessels of leg
Microvascular diseases: small vessels
- retinopathy
- diabetic kidney disease (nephropathy)
- peripheral neuropathy (loss of sensation/tingling) & increased risk of foot infections and amputations
- autonomic neuropathy (gastroparesis, loss of bladder control, erectile dysfunction)
Diabetes is the top cause of what three complications? and what is the primary cause of death of DM patients?
- lower extremity amputations
- kidney failure
- blindness
- primary cause of death is CVD - occurs at 2-4 times more than regular ppl’s cause of death
ASCVD prevention for DM patient
Can give ASA 75-162 mg/day - typically just 81 mg/day for secondary prevention only (ex: after MI)
Can give clopidogrel 75 mg daily if they have an allergy to ASA
DM patient with CAD or PAD can be given what to prevent complications
ASA 81 mg/day PLUS xarelto
How can we reduce risk of secondary pre-eclampsia in pregnancy
- Give ASA 81 mg daily starting after 12 weeks in women at risk for preeclampsia
How can we monitor for diabetic retinopathy
Patients should get an eye exam using dilation at the time of DM diagnosis
- If they have retinopathy; repeat eye exams every year
- If they don’t; repeat eye exams every 1-2 years
What vaccinations do DM patients
Hepatitis B virus
Pneumonia
Influenza
Monitoring parameters for preventing neuropathy and when we treat what can we give?
- 10 g monofilament exam + another sensation test (vibration, temp, or pinprick, etc.) annually
- comprehensive foot exam at least annually –> refer to podiatrist if high risk
Treat: pregabalin, gabapentin, or duloxetine
How can we counsel a DM patient about foot care
- Wash, dry, and examine feet daily
- Moisturize the top and bottom of feet, BUT NOT BETWEEN THE TOES
- Each office visit, they should take off shoes and have their feet checked
- Annual foot checks from podiatrist
-Trim toe nails with a nail file! don’t cut them if possible because it will leave sharp edges from using a nail clipper. If you cut straight across, file the edges so that they dont dig into the skinW - Wear socks and shoes
- avoid crossing legs for too long which can cut off circulation
- Elevate feet when sitting
When do we give high intensity or moderate intensity statins to patients with DM?
HIGH INTENSITY STATIN if
DM + ASCVD or if
Age 50-75 yrs AND multiple ASCVD risk factors (smoking/large secondary smoke exposure, lack of physical activity, high LDL cholesterol, HTN, unhealthy diet, obesity, etc. (atorvastatin 40-80 mg or rosuvastatin 20-40 mg daily)
MODERATE INTENSITY STATIN if
if DM + age 40-75 yrs with no ASCVD or
if DM + age < 40 years + ASCVD risk factors
(ex: Atorvastatin 10-20 mg, Lovastatin 40-80 mg, Pitavastatin 2-4 mg, Pravastatin 40-80 mg, Rosuvastatin 5-10 mg, Simvastatin 20-40 mg)
When do we need to add on additional treatment for DM patient’s cholesterol after being maximally tolerated on statins
- Ezetimibe can be added for patients whose 10 year ASCVD risk is > 20%
- Icosapent ethyl (Vascepa) can be added if LDL is controlled, but the TG’s are 135-499 mg/dL
What labs should we get to monitor cholesterol in DM patients and how often?
Lipid panel annually and 4-12 weeks after starting statin or increasing dose
How often/ what lab should we use monitor kidneys in DM and how should we treat
- Urine albumin and eGFR test annually if normal kidney function
- twice annually if eGFR 30-60 ml/min/1.73 m^2 or urine albumin >/= 300
If albuminuria: Dx as eGFR of >/= 30 in 24 hrs or urine albumin to creatine ratio (UACR) >/= 30 mg/g
TREAT with ACEI or ARB
if eGFR >/=25 ml/min/1.73 m^2 AND urine albumin >/= 300
TREAT with SGLT2 or finerenone if unable to use
What are our blood pressure goals for DM patients? and how do we treat when they also have CAD or HTN w or w/o albuminuria ?
if ASCVD risk >/= 15%: BP goal <130/80 mmHg
if ASCVD risk < 15% BP goal <140/90 mmHg is acceptable
TREAT:
if no albuminuria: thiazide, DHP CCB, ACEI or ARB
if albuminuria or CAD: ACEI or ARB
(so basically if someone has DM + HTN, use ACEi or ARB and consider contraindications)
What are natural products used to decrease BG in T2DM with low or minimal efficacy
Main ones: Cassia cinnamon, alpha lipoic acid, chromium,
others: magnesium, panax/american ginseng
What is our starting treatment for DM
Metformin + lifestyle changes (diet, weight loss, etc.)
After starting Tianna’s initial treatment for DM with metformin, patient is still not at goal A1C, and has no ASCVD, HF, or CKD, what’s next/what do you consider?
Add any class of DM meds considering patient specific risk factors :
Least hypoglycemia risk: DPP-4i’s, GLP1a’s, SGLT2i’s, TZD’s
Highest weight loss: GLP1a’s , SGLT2i’s
Lowest cost: SU’s or TZD
if still not at A1c goal: try a different class that hasn’t been started
After starting Tianna’s initial treatment for DM with metformin, the patient has ASCVD or is at high risk. What’s next/what do you consider?
What if she’s above A1c goal after that?
Regardless of A1C:
start GLP1a or SGLT2i with benefit
GLP1a’s: semaglutide (subQ), liraglutide, dulaglutide
SGLT2i’s: canaglaflozin, empagliflozin
if above A1c goal: try the alt. GLP1a or SGLT2i or TZD, basal insulin, Su, or DDP4i
After starting Tianna’s initial treatment for DM with metformin, the patient has HF. What’s next/what do you consider?
Regardless of A1c%, start SGLT2i’s with benefit: Dapagliflozin, empagliflozin, potentially canagliflozin
After starting Tianna’s initial treatment for DM with metformin, the patient has CKD. What’s next/what do you consider?
Regardless of A1c%:
Start a GLP1a or SGLT2 with benefit (SGLT2’s are preferred if albuminuria)
SGLT2i (canagliflozin - DKD benefit, dapagliflozin - CKD benefit, and potentially empagliflozin) or GLP1a (semaglutide- subQ, dulaglutide, liraglutide)
What are high risk ASCVD factors in DM patients
- age >/= 55
- coronary, carotid, or lower extremity artery stenosis >50%
- Left ventricular hypertrophy
if they have any of these, they should be treated with an appropriate SGLT2i (canagliflozin, empagliflozin) or GLP1a (semaglutide, dulaglutide, liraglutide)
What DM medication combination should be avoided?
DPP4i + GLP1a (overlapping MOAs) or SU + Insulin (hypoglycemia risk)
What therapy do we initiate if newly diagnosed DM patient John’s A1c is 8.5-10%?
We will start metformin + another non-insulin drug depending on his factors (ASCVD, ASCVD risk factors, HF, CKD) if no comorbidities, consider patient specific factors (cost, risk of hypoglycemia, and risk of weight gain)
Regardless of A1c, if newly diagnosed DM patient has ASCVD or high risk factors, or CKD, or HF, how should we initiate therapy
consider appropriate and SGLT2’s, GLP1a’s to add with metformin
When do we initiate insulin therapy
- initially ONLY if hyperglycemia is severe (A1c>10%, BG ≥ 300 mg/dl
True or false: GLP1’s are preferred over insulin in instances where we need an injectable medication to lower A1C
True because they have the same A1c lowering ability, but they don’t cause weight gain like insulin - they actually help with weight loss. They are more expensive than insulin though.
ex: semaglutide subQ
Whenever A1c remains above goal in our patients, what should we do?
Consider adding one more DM medication that is beneficial for their comorbidity or their patient specific factor.
Avoid combo of GLP1a, SU + insulin + DPP4i
What anti-diabetic drug class should be avoided in patients with heart failure
Thiazides or “glitazones”
Which two drugs should not be used in patients with bladder cancer
dapagliflozin (SGLT2-i) and pioglitazone (Thiazolidinedione - TZD)
Which drug should you never pick if a patient has had history or foot problems (ulcers, neuropathy, etc.)
Canagliflozin because it’s black box warning for causing leg and foot amputations
Which drug class has increased risk of ketoacidosis at BG < 250 mg/dl and what should we do if Roberta is on this drug before her surgery
SGLT2-i’s - we need to discontinue this before patients surgery
Which part of the nephron do SGLT2-i’s work on
The proximal convoluted tubule in the nephron and it blocks reabsorption of glucose back into the body, instead it’s excreted out.
What is the ICR
Insulin to Carb Ratio - helps us understand how many carbs one unit of insulin will cover for the meal they are about to eat.
Someone who’s preprandial BG is not at goal before their meal will need to calculate ICR and correction factor.
How to calculate ICR for Regular Insulin
ICR= 450/TDD (including non-regular daily insulin)
(round to nearest whole #)
How to calculate ICR for Rapid Acting Insulin
ICR= 500/TDD (including non rapid acting insulin) (round to nearest whole #)
What is correction factor
It is also known as insulin sensitivity factor. This is used when the persons pre-meal BG is not within goal range. This tells us how much the BG will be lowered in mg/dL by 1 unit of insulin. They then will need to calculate a correction dose to bring the BG down to goal.
How to calculate correction factor for regular insulin
1500/TDD = correction factor in mg/dL for 1 unit of regular insulin (round to nearest whole #)
Correction Factor formula for rapid acting insulin
1800/TDD = correction factor in mg/dL for 1 unit of rapid acting insulin (round to nearest whole #)
Correction dose formula
(Blood glucose now - target BG)/correction factor = correction insulin dose for both regular and rapid acting types (round to nearest whole # and add to normal meal time insulin dose)
Target BG for most patients in the hospital
140 - 180 mg/dL - treatment should be proactive to maintain BG in this range rather than just treating when BG is high
True or false: using sliding scale insulin alone to control BG in the hospital is acceptable
False: This is a reactionary method for controlling BG, which we need to avoid because it’s dangerous and not patient specific. We need to prevent high BG rather than only treating it. So instead, it’s better to use:
Basal + Bolus + correction doses strategy is preferred if patients are eating adequately
Basal and correction dose preferred if patients are not eating adequately
Which insulin is preferred on sliding scales bc it drops BG the fastest
Rapid acting preferred over regular insulin, but its more expensive
What is Hemoglobin A1c
It’s a measure of percentage of RBC’s are glycosylated because when the BG is high, Hgb is super sticky and makes glucose stick onto the RBCs. So A1C didn’t use to be, but has become a way to Dx DM.
The reason we only test it every 3 months is because of the lifespan of the RBC
What is Hemoglobin A1c
It’s a measure of percentage of RBC’s are glycosylated because when the BG is high, Hgb is super sticky and makes glucose stick onto the RBCs. So A1C didn’t use to be, but has become a way to Dx DM.
Whats a counseling point we can give to DM patients to test temperature to make sure they dont burn their feet if they have lost sensation
elbow test; allows them to dip elbow in water or whatever so they know if its too hot or not
Which insulins have cardiovascular benefit
Glargine (U-100) or Degludec
T or F: If a patient is having lots of GI symptoms on IR metformin, switching to XR metformin can help
True
What should you do if a patient is on an SGLT2i and they are expecting to have a surgery soon?
They need to discontinue the SGLT2i 3 days prior to the surgery because SGLT2i’s can cause a ketoacidosis even at normal blood sugars after surgery
